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- W1982294185 abstract "BARTTER and associates,<sup>1</sup>in 1962, described two patients who had hyperplasia and hypertrophy of the juxtaglomerular apparatus, hyperaldosteronism, hypokalemic metabolic alkalosis, and normal blood pressure. Since that time, many cases have been reported with these findings, and the entity has come to be called Bartter syndrome. The observation that these patients showed marked resistance to the pressor effects of infused exogenous angiotensin caused Bartter and his colleagues to hypothesize that the syndrome was the result of a primary inability of the vasculature of arterial circulation to respond to the pressor effects of angiotensin. This, they reasoned, resulted in a slack circulation sensed by the kidney as a contraction of the effective arterial volume; the kidney in turn increased the production of renin, with consequent increase in circulating levels of angiotensin II. But the latter had no effect on the state of arterial contraction, since the arterial vessels were unable" @default.
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- W1982294185 date "1975-11-17" @default.
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- W1982294185 title "The Pathophysiology of Bartter Syndrome" @default.
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- W1982294185 doi "https://doi.org/10.1001/jama.1975.03260200074030" @default.
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